Even with the intensive efforts by public health programs to control and prevent it, non-typhoidal Salmonella (NTS) infection remains an important public health challenge. It is responsible for approximately 150 million illnesses and 60,000 deaths worldwide annually. NTS infection poses significant risks with high rates of morbidity and mortality, leading to potential short- and long-term complications. There is growing concern among health authorities about the increasing incidence of antimicrobial resistance, with multidrug resistance totaling 22.6% in Europe, highlighting an urgent need for new therapeutic approaches. Our review aims to provide a comprehensive overview of NTS infection. We outline the molecular mechanisms involved in the pathogenesis of NTS infection, as well as the events leading to invasive NTS infection and the subsequent complications associated with it. Given the widespread implications of antimicrobial resistance, our review also presents the global landscape of resistance, including multidrug resistance, and delve into the underlying mechanisms driving this resistance. The rising rates of antibiotic resistance frequently lead to treatment failures, emphasizing the importance of investigating alternative therapeutic options. Therefore, in this review we also explore potential alternative therapies that could offer promising approaches to treating NTS infections.

The increasing incidence of antibiotic resistance in bacteria is a major problem in terms of therapeutic options, especially in immunocompromised patients, such as patients from intensive care units (ICUs), HIV-positive patients, patients with malignancies or transplant patients. Commensal bacteria, especially anaerobes, serve to maintain microbial stability by preventing overpopulation with pathogenic bacteria. In immunocompromised patients, microbiota imbalance caused by antibiotic therapy and decreased host immunity favors intestinal overpopulation with pathogenic species, leading to increased bacterial translocation and susceptibility to systemic infections. Infections with multidrug-resistant (MDR) bacteria pose major challenges to the establishment of appropriate treatment and lead to increased mortality. Asymptomatic colonization with MDR bacteria usually precedes infection and tends to persist for long periods of time, and in immunocompromised patients, colonization with MDR bacteria is a risk factor for systemic infections. This review aims to assess the relation between colonization and infection with MDR bacteria in immunocompromised patients such as ICU patients, HIV-positive patients and cancer patients and to identify the prevalence and patterns of MDR bacterial colonization and infection in this category of patients.

Enteric fever is caused by Salmonella enterica serovar Typhi (S. Typhi) and Salmonella enterica serovar Paratyphi (S. Paratyphi) A, B, and C. Globally, an estimated 11 to 21 million cases of typhoid and paratyphoid fever occur annually, with approximately 130,000–160,000 deaths, most of which are reported in South/Southeast Asia and sub-Saharan Africa. The antibiotic susceptibility of S. Typhi strains varies between countries within broad limits, from 3% to 97% for ampicillin, 9% to 95% for ciprofloxacin, 4% to 94% for chloramphenicol (India vs. Pakistan), and 0% to 99% for ceftriaxone (India vs. Iraq). With S. Typhi increasingly exhibiting resistance to antibiotics, vaccination becomes an essential preventive measure. Currently, three vaccines are licensed for typhoid fever: the typhoid conjugate vaccine (TCV), live-attenuated oral vaccine Ty21a (Ty21a), and Vi capsular polysaccharide vaccine (Vi-CPS). While no specific vaccine exists for paratyphoid fever, the genetic and antigenic similarities between S. Paratyphi and S. Typhi offer potential for the development of such a vaccine. Early studies show promising results, demonstrating both safety and immunogenicity in preclinical trials. Whole genome sequencing (WGS) provides a powerful tool for assigning genotypes, identifying plasmids, comparing genetic elements, and investigating molecular factors that contribute to antibiotic resistance and virulence.

Early life represents a critical developmental programming window during which nutrition and microbial exposures shape long-term physiological function. Feeding mode is a major determinant of infant gut microbiota assembly and metabolic activity. This narrative review synthesizes current evidence comparing breastfeeding (BF) and formula feeding in relation to microbial composition, functional capacity, and immune programming during the preweaning and early postweaning periods. BF may support a relatively stable, bifidobacteria-dominated microbiota enriched in pathways involved in carbohydrate utilization, vitamin biosynthesis, and immune modulation. Human milk oligosaccharides, secretory IgA, lactoferrin, and milk-associated microbes collectively guide microbial succession, enhance barrier integrity, and support immune tolerance. In contrast, formula-fed infants typically exhibit greater microbial diversity, earlier transition toward adult-like profiles, and increased abundance of facultative anaerobes, alongside the enrichment of pathways related to bile acid and amino acid metabolism. Microbiota patterns in formula-fed infants are further influenced by formula composition, including protein load, lipid structure, and supplementation with prebiotics, probiotics, and human milk oligosaccharide analogues. Although advances in formula design have reduced compositional gaps, functional differences in microbial stability and immune programming persist. Recognizing early infancy as a sensitive programming window underscores the need for microbiome-informed nutritional strategies and longitudinal, multi-omics research to clarify causal mechanisms and optimize early-life interventions.

Background/Objectives: Healthcare-associated infections caused by multidrug-resistant (MDR) bacteria pose a significant and growing public health challenge, particularly in high-risk settings such as Intensive Care Units (ICUs). Colonization is often asymptomatic but can precede infection and contribute to hospital outbreaks, making early detection critical for infection control and containment. The aim of the study is to evaluate the antibiotic susceptibility patterns of MDR bacteria involved in colonization and/or infection among patients admitted to the ICU at a tertiary care hospital in Northeastern Romania and to investigate the relationship between MDR bacterial colonization and subsequent infection. Methods: A total of 118 patients from ICU were included in this study and a total of 609 bacterial strains were isolated, involved in both colonization and infection, with multiple isolates per patient included if obtained from different sites or time points. Results: A predominance of Gram-negative bacilli was found to be involved in both colonization and infection in the ICU, with Acinetobacter baumannii (n = 146; 26.64%), Klebsiella pneumoniae (n = 146; 26.64%), Escherichia coli (n = 60; 10.95%), and Pseudomonas aeruginosa (n = 56; 10.22%) as the main bacteria involved in colonization, and A. baumannii (n = 23; 37.7%), K. pneumoniae (n = 19; 31.1%), and P. aeruginosa (n = 15; 24.6%) as the main bacteria involved in infections. The study revealed a high diversity of antibiotypes among K. pneumoniae (43 distinct antibiotypes), E. coli (35 distinct antibiotypes) and P. aeruginosa (27 distinct antibiotypes). In contrast, only 6 antibiotypes were identified for A. baumannii, with most strains belonging to a single dominant antibiotype. For K. pneumoniae, E. coli and A. baumannii, infections mainly involved the same antibiotype as that found in colonization, while infections with P. aeruginosa were often linked to different antibiotypes than those involved in colonization. Conclusions: This study demonstrates a high colonization-to-infection link among ICU patients in a Northeastern Romanian tertiary care hospital, and these findings underscore the importance of systematic colonization screening to identify patients at high risk in ICU settings.

Even with significant advances in therapeutic interventions and monitoring protocols, cystic fibrosis (CF) remains a critical pediatric health challenge affecting respiratory function and long-term patient outcomes. CF, caused by mutations in the CFTR gene, disrupts normal mucociliary clearance and creates conditions for chronic respiratory infections. The disorder affects individuals globally, with pediatric patients facing particularly complex microbial challenges that evolve throughout childhood growth. CF poses significant risks with progressive lung function decline and increased mortality, leading to potential short- and long-term respiratory complications. There is a growing concern among clinicians about the dynamic nature of airway microbial communities, with classical pathogens like Pseudomonas aeruginosa and Staphylococcus aureus showing sequential emergence patterns that complicate treatment strategies, highlighting an urgent need for microbiome-informed therapeutic approaches. Our review aims to provide a comprehensive overview of airway microbiome evolution in pediatric CF patients. We outline the molecular and ecological mechanisms involved in microbial community progression, as well as the age-related trajectories leading to pathogen-dominated ecosystems and the subsequent complications associated with microbial dysbiosis. Given the widespread implications of disrupted microbial balance on disease progression, our review also presents the temporal landscape of airway microbiome changes, including age-related microbial succession patterns, and explores the underlying mechanisms driving these ecological shifts. The progressive nature of microbial simplification frequently leads to treatment challenges, emphasizing the importance of investigating microbiome-targeted therapeutic interventions. Therefore, in this review, we also explore established therapeutic strategies, including CFTR modulators and probiotics, which could offer promising approaches to maintaining microbial balance and improving outcomes in pediatric CF patients.